THE GILL CALCIUM-TRANSPORT CYCLE IN RAINBOW-TROUT IS CORRELATED WITH PLASMA-LEVELS OF BIOACTIVE, NOT IMMUNOREACTIVE, STANNIOCALCIN

Stanniocalcin (STC) is an inhibitor of gill Ca2+ transport that is produced by the corpuscles of Stannius, endocrine glands in bony fish. In young rainbow trout (Oncorhynchus mykiss), there are cyclical changes in the rate of gill Ca2+ transport, with alternating phases of accelerated and reduced uptake every 14 days. Previous studies by our laboratory have established that the responsiveness of young trout to the inhibitory effects of exogenous STC is dependent on this cycle. Trout are highly responsive to STC at peaks of Ca2+ uptake and unresponsive at nadirs, which has led us to suggest that the gill Ca2+ transport cycle may be regulated by a reciprocal cycle in the levels of plasma STC. In this report, we have further characterized the gill Ca2+ transport cycle in salmonids and investigated the role of STC in its regulation. Our results showed that the cycle is synchronous and is likely a characteristic feature in all salmonids but that it varies in amplitude between species. Surprisingly, we observed no correlation between circulating levels of radioimmunoassayable STC and the rate of gill Ca2+ transport in trout. To address this apparent contradiction, trout fry were passively immunized with STC antiserum to determine if there were variable amounts of bioactive STC in the circulation, at times when trout were either more or less sensitive to exogenous STC. We observed that during the times when trout were responsive to STC treatment (i.e., cycle peaks), passive immunization had no effect on the rate of gill Ca2+ transport in fish from the same population, indicating that there were low levels of bioactive STC in the circulation. Conversely, during times when trout were insensitive to exogenous STC (i.e., cycle nadirs), passive immunization significantly raised the rate of transport through neutralization of endogenous STC, indicating that there were high levels of bioactive hormone in the experimental population as a whole. The results suggest that the cycle is controlled by reciprocal changes in the amount of bioactive, but not immunoreactive, STC. As the trout were capable of responding or were already responding to the effects of STC at all given times, this would rule out changes in the number of functional STC receptors as an explanation for these findings. As a consequence, it appears that some factor is modifying the extent to which circulating or secreted STC is biologically active and is therefore exerting a higher level of control over gill Ca2+ transport.